Labor and Parturition

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Powerful contractions of the uterus are needed to expel the fetus in the sequence of events called labor. These uterine contractions are known to be stimulated by two agents: (1) oxytocin, a polypeptide hormone produced in the hypothalamus and released by the posterior pituitary (and also produced by the uterus itself), and (2) prostaglandins, a class of cyclic fatty acids with paracrine functions produced within the uterus. The particular prostaglandins (PGs) involved are PGF2a and PGE2. Labor can indeed be induced artificially by injections of oxytocin or by insertion of prostaglandins into the vagina as a suppository.

Although labor is known to be stimulated by oxytocin and prostaglandins, the factors responsible for the initiation of labor are incompletely understood. In all mammals, labor is initiated by activation of the fetal adrenal cortex. In mammals other than primates, the fetal hypothalamus-anterior pituitary-adrenal cortex axis sets the time of labor. Corticosteroids secreted by the fetal adrenal cortex then stimulate the placenta to convert progesterone into estrogens. This is significant because progesterone inhibits activity of the myometrium, while estrogens stimulate the ability of the myometrium to contract. However, the initiation of labor in humans and other primates is more complex. Progesterone levels do not fall because the human placenta cannot




Hypothalamus CRH


Placenta Secreting Progestrone




Placental CRH




Posterior pituitary


+ Prostagland E2

Prostaglandin F2a

1. Increased receptors for oxytocin and prostaglandins

2. Increased gap junctions in myometrium

Placental CRH

Childbirth Feedback Loop


■ Figure 20.52 Labor in humans. The fetal adrenal gland secretes dehydroepiandrosterone sulfate (DHEAS) and cortisol upon stimulation by CRH (corticotropin releasing hormone) and ACTH (adrenocorticotropic hormone). In turn, cortisol stimulates the placenta to secrete CRH, producing a positive feedback loop. The DHEAS is converted by the placenta into estriol, which is needed, together with prostaglandins and oxytocin, to stimulate the myometrium of the mother's uterus to undergo changes leading to labor. The plus signs emphasize activation steps critical to this process.

convert progesterone into estrogens; it can only make estrogen when it is supplied with androgens from the fetus (fig. 20.51).

The fetal adrenal lacks a medulla, but the cortex itself is composed of two parts. The outer part secretes cortisol, as does the adult adrenal cortex. The inner part, called the fetal adrenal zone, secretes the androgen dehydroepiandrosterone sulfate (DHEAS). Once the DHEAS from the fetus travels to the pla centa, it is converted into estrogens. The rising secretion of estrogens (primarily estriol), in turn, stimulates the uterus to (1) produce receptors for oxytocin; (2) produce receptors for prostaglandins; and (3) produce gap junctions between myome-trial cells in the uterus (fig. 20.52). The increase in oxytocin and prostaglandin receptors makes the myometrium more sensitive to these agents. The gap junctions (which function as electrical synapses—see chapter 7) help to synchronize and coordinate the contractions of the uterus.

This chain of events may be set in motion by the placenta, through its secretion of corticotropin-releasing hormone (CRH). The CRH produced by the placenta, like the CRH produced by the hypothalamus (chapter 11), stimulates the anterior pituitary to secrete ACTH (adrenocorticotropic hormone). There is also evidence for CRH receptors in the fetal adrenal gland, suggesting that the CRH produced by the placenta can itself stimulate adrenal secretion. Thus, CRH from the placenta directly and indirectly (via stimulation of ACTH secretion) stimulates the fetal adrenal cortex to secrete cortisol and DHEAS.

The secretion of cortisol from the fetal adrenal cortex helps to promote maturation of the fetus's lungs; it also stimulates the placenta to secrete CRH, resulting in a positive feedback loop that also increases secretion of DHEAS (fig. 20.52). The placenta can then convert the increased amounts of DHEAS into increased amounts of estriol. The estriol, in turn, activates the myometrium to become more sensitive to oxytocin and prostaglandins, as previously described. Thus, the chain of events the culminates in parturition may be set in motion by the placenta's secretion of CRH. How this "placental clock" is timed, however, is not currently understood.

Studies in rhesus monkeys demonstrate that there is a rise in the oxytocin concentration of the mother's plasma during the night, but not during the day. The uterus also produces oxytocin, which may act as a paracrine regulator along with prosta-glandins to stimulate contractions and supplement the actions of the oxytocin released by the posterior pituitary. The concentration of oxytocin receptors in the myometrium increases dramatically as a result of estrogen stimulation, as previously described, making the uterus more sensitive to oxytocin. These effects culminate in parturition, or childbirth.

Following delivery of the baby, oxytocin is needed to maintain the muscle tone of the myometrium and to reduce hemorrhaging from uterine arteries. Oxytocin may also play a role in promoting the involution (reduction in size) of the uterus following delivery; the uterus weighs about 1 kg (2.2 lb) at term but only about 60 g (2 oz) by the sixth week following delivery.

Pectoralis minor

Deep fascia


J V;


■" i * r


M 2


Parturition Ampulla Breast

Secondary tubules



■ Figure 20.53 The structure of the breast and mammary glands. (a) A sagittal section and (b) an anterior view partially sectioned.

Genetic screening of neonates (newborns) is done in hospitals using only a drop of blood obtained by pricking the foot. Most of these blood tests do not involve DNA or chromosomal testing, yet they can detect a variety of genetic disorders, including phenylketonuria, hypothyroidism, cystic fibrosis, hemoglobin disorders such as sickle-cell anemia, and many others. Also, umbilical cord blood banking may be performed after birth. As described in chapter 13, this is done because the umbilical cord blood contains a high concentration of hematopoietic stem cells, which can replenish the blood cell forming ability of bone marrow that has been damaged (by chemotherapy of leukemia, for example). Indeed, one unit of cord blood can reconstitute a person's entire hematopoietic system. Using banked umbilical cord blood for transplantation later in life minimizes immunological rejection.

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  • abrha temesgen
    How to increase prostaglandin and oxytocin release in humans?
    8 years ago
  • Kaitlyn Morrison
    Does oxytocin make prostaglandin?
    8 years ago
  • paolo
    What is physiogy of human labour?
    8 years ago
  • conrad
    Where prostaglandin is produced at the placenta site?
    8 years ago
  • Robert
    Does placental crh stimulate fetal lungs?
    8 years ago
  • Marisa
    Does estrogen stimulate oxytocin secretion during sexual arousal?
    8 years ago
    What is the function and physiology of parturition?
    8 years ago
  • bercilac
    Does estrogen stimulates the mother's uterus during parturition?
    7 years ago
  • James
    Which Two Agents Stimulate Uterine Contraction Labor In Humans?
    5 years ago
  • Marja
    How to induce partirutionin humans?
    4 years ago
  • futsum
    How does oxytocin make the myometrium contract?
    3 years ago
  • Linda
    What is labour and parturition in human ?
    3 years ago
  • ida
    What is patruition in human?
    2 years ago
  • Kasey
    How does activation of fetal adrenal gland initiate labor?
    2 years ago

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